Mechanisms of reoxygenation-induced calcium overload in cultured chick embryo heart cells.
Mechanisms of reoxygenation-induced calcium overload in cultured chick embryo heart cells.
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培养鸡胚心脏细胞复氧诱导钙超载的机制。
DOI：
10.1152/ajpheart.1988.254.6.h1133
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Marsh,JD
中科院分区：
文献类型：
--
作者：
Murphy,JG;Smith,TW;Marsh,JD
我们研究了缺氧后再氧合过程中钙进入培养心肌细胞的机制。从卵内10天的心脏制备鸡胚心室细胞的单层培养物。将细胞暴露于缺氧条件（PO 2小于1.5 Torr），然后在不存在和存在Ca通道依赖性Ca进入和Na-Ca交换的调节剂的情况下检查随后的再氧合期间的45 Ca摄取。还检查了自由基清除酶对Ca进入的调节。缺氧120 min后复氧使钙含量从1.9 nmol/mg蛋白增加到6.1 nmol/mg蛋白在复氧前加入维拉帕米（10（-5）M），使钙超载降至3.1 +/- 0.2 nmol/mg蛋白质复氧30 min后加入维拉帕米和BAY K 8644对钙内流无明显影响（P> 0.05）。缺氧复氧后，细胞内24 Na含量由对照组的70 nmol/mg蛋白增加到157 nmol/mg蛋白（P <0.05），有利于Ca通过Na-Ca交换进入细胞。Dichlorobenzamil显着改善复氧诱导的钙超载，过氧化氢酶和超氧化物歧化酶。我们的结论是，再氧诱导的钙超载是不太可能发生通过钙通道。它部分通过Na-Ca交换发生，并通过酶促O2自由基清除剂显著改善。
We examined mechanisms by which Ca enters cultured myocardial cells during posthypoxic reoxygenation. Monolayer cultures of chick embryo ventricular cells were prepared from hearts 10 days in ovo. Cells were exposed to hypoxic conditions (PO2 less than 1.5 Torr), and 45Ca uptake during subsequent reoxygenation was then examined in the absence and presence of modulators of Ca channel-dependent Ca entry and Na-Ca exchange. Modulation of Ca entry by free radical-scavenging enzymes was also examined. Hypoxia for 120 min followed by reoxygenation increased Ca content from 1.9 to 6.1 nmol/mg protein (P less than 0.05) at 30 min. Verapamil (10(-5) M) added before reoxygenation reduced Ca overload to 3.1 +/- 0.2 nmol/mg protein (P less than 0.05), but both verapamil and BAY K 8644 were without effect on modulating Ca entry if added 30 min after reoxygenation. 24Na content of cells increased from 70 nmol/mg protein in control cells to 157 nmol/mg protein (P less than 0.05) after hypoxia and reoxygenation, favoring Ca entry via Na-Ca exchange. Dichlorobenzamil significantly ameliorated reoxygenation-induced Ca overload, as did catalase and superoxide dismutase. We conclude that reoxygenation-induced Ca overload is unlikely to occur via the Ca channel. It occurs in part via Na-Ca exchange and is substantially ameliorated by enzymatic O2 free radical scavengers.